This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. In 2010 we concluded the studies for our parent R01 (Functional Neuroanatomy of the Basolateral Amygdala) and using preliminary data generated from the parent grant we successfully applied to NIH for continuing R01 funding (Fear and Dopamine in the Basolateral Amygdala). Based on our previous studies, we knew that a subpopulation of BLA interneurons, the parvalbumin containing cells, were key regulators of synchronized neural activity in the BLA. The results of this study were submitted to the Journal of Physiology [Lond.] and are currently being revised (Jasnow et al., in revision). The results of our previous studies had also suggested that the excitability of the parvalbumin interneurons was tightly controlled by expression of the transient outward potassium current, IA. These channels form macromolecular complexes with chaperone molecules, including the potassium channel interacting proteins (KChIPs). We have examined the relative distribution of KChIPs (KChIP1 [unreadable]KChIP4) in the BLA and noted that KChIP1 was selectively expressed in a subpopulation of neurons. We have extended this study to show that KChiP1 is almost exclusively expressed in the population of parvalbumin expressing interneurons. In addition, we completed our study into the dopamine-dependence of LTP induction in principal neurons of the BLA. Moreover, we extended these studies to show that a synaergistic interaction between dopamine, brain derived nerve growth factor, and synaptically released zinc, are a prerequisite for LTP induction, and by extrapolation fear memory formation.